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J. Biol. Chem., Vol. 278, Issue 19, 17036-17043, May 9, 2003
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From the Mucus hypersecretion and persistent airway
inflammation are common features of various airway diseases, such as
asthma, chronic obstructive pulmonary disease, and cystic fibrosis. One
key question is: does the associated airway inflammation in
these diseases affect mucus production? If so, what is the underlying
mechanism? It appears that increased mucus secretion results
from increased mucin gene expression and is also frequently accompanied
by an increased number of mucous cells (goblet cell
hyperplasia/metaplasia) in the airway epithelium. Many studies on mucin
gene expression have been directed toward Th2 cytokines such as
interleukin (IL)-4, IL-9, and IL-13 because of their known
pathophysiological role in allergic airway diseases such as asthma.
However, the effect of these cytokines has not been definitely linked
to their direct interaction with airway epithelial cells. In our study,
we treated highly differentiated cultures of primary human
tracheobronchial epithelial (TBE) cells with a panel of cytokines
(interleukin-1
Stimulation of Airway Mucin Gene Expression by Interleukin
(IL)-17 through IL-6 Paracrine/Autocrine Loop*
,,,
Center for Comparative Respiratory Biology
and Medicine and Division of Pulmonary and Critical Care Medicine,
University of California, Davis, California 95616, § Institute of Environmental Health Sciences, Wayne State
University, Detroit, Michigan 48201, and ¶ GlaxoSmithKline
Pharmaceuticals, King of Prussia, Pennsylvania 19406
, 1
, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 15, 16, 17, 18, and tumor necrosis factor ). We found that IL-6 and
IL-17 could stimulate the mucin genes, MUC5B and
MUC5AC. The Th2 cytokines IL-4, IL-9, and IL-13 did not
stimulate MUC5AC or MUC5B in our experiments. A
similar stimulation of MUC5B/Muc5b expression by IL-6 and
IL-17 was demonstrated in primary monkey and mouse TBE cells. Further investigation of MUC5B expression demonstrated that
IL-17's effect is at least partly mediated through IL-6 by a
JAK2-dependent autocrine/paracrine loop. Finally, evidence
is presented to show that both IL-6 and IL-17 mediate MUC5B
expression through the ERK signaling pathway.
*
This work was supported by National Institutes of Health
Grants HL35635, ES06230, ES09701, AI50496, ES00628, ES04699, and ES05707, California Tobacco-Related Disease Research Program 10RT-0262, and a grant from Glaxo/Smith Kline/Welcome Inc.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Center for
Comparative Respiratory Biology and Medicine, Surge 1 Annex, Room 1121, University of California at Davis, One Shields Ave., Davis, CA 95616. Tel.: 530-752-2648; Fax: 530-752-8632; E-mail: rwu@ucdavis.edu.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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